Regulation of hepatic glutamine metabolism during exercise in the dog
Department of Molecular Physiology and Biophysics, Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 The goal of this study was to determine how liver glutamine (Gln) metabolism adapts to acute exercise in the 18-h-fasted dogs ( n = 7) and i...
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Published in | American journal of physiology: endocrinology and metabolism Vol. 275; no. 4; pp. E655 - E664 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.10.1998
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Subjects | |
Online Access | Get full text |
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Summary: | Department of Molecular Physiology and Biophysics, Diabetes Research
and Training Center, Vanderbilt University School of Medicine,
Nashville, Tennessee 37232
The goal of this
study was to determine how liver glutamine (Gln) metabolism adapts to
acute exercise in the 18-h-fasted dogs ( n = 7) and in dogs that were glycogen
depleted by a 42-h fast ( n = 8). For
this purpose, sampling (carotid artery, portal vein, and hepatic vein)
and infusion (vena cava) catheters and Doppler flow probes (portal
vein, hepatic artery) were implanted under general anesthesia. At least
16 days later an experiment, consisting of a 120-min equilibration
period, a 30-min basal sampling period, and a 150-min exercise period
was performed. At the start of the equilibration period, a
constant-rate infusion of
[5- 15 N]Gln was
initiated. Arterial Gln flux was determined by isotope dilution. Gut
and liver Gln release into and uptake from the blood were calculated by
combining stable isotopic and arteriovenous difference methods. The
results of this study show that 1 )
in the 18-h-fasted dog, ~10% and ~35% of the basal Gln appearance in arterial blood is due to Gln release from the gut and liver, respectively, whereas ~30% and ~25% of the basal Gln
disappearance is due to removal by these tissues;
2 ) extending the fast to 42 h does
not affect basal arterial Gln flux or the contribution of the gut to
arterial Gln fluxes but decreases hepatic Gln release, causing a
greater retention of gluconeogenic carbon by the liver; 3 ) moderate-intensity exercise
increases hepatic Gln removal from the blood regardless of fast
duration but does not affect the hepatic release of Gln; and
4 ) Gln plays an important role in channeling nitrogen into the ureagenic pathway in the basal state, and
this role is increased by ~80% in response to exercise. These studies illustrate the quantitative importance of the splanchnic bed
contribution to arterial Gln flux during exercise and the ability of
the liver to acutely adapt to changes in metabolic requirements induced
by the combined effects of fasting and exercise.
liver; gastrointestinal tract; stable isotope; nitrogen; amino
acids |
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Bibliography: | S20 1997084555 |
ISSN: | 0002-9513 0193-1849 2163-5773 1522-1555 |
DOI: | 10.1152/ajpendo.1998.275.4.e655 |